IOSR Journal of Dental and Medical Sciences (IOSR-JDMS)

e-ISSN: 2279-0853, p-ISSN: 2279-0861.Volume 13, Issue 6 Ver. II (Jun. 2014), PP 51-54
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Changing Perspectives in Classifications of Hypertensive

Retinopathy.
Amit Chopra , Amit Sharma , Surat Singh , Vishwajyoti Bahl
Department of Ophthalmology , MM Medical College, Kumarhatti , Solan , India.

Abstract: Hypertensive retinopathy represents the ophthalmic findings of end organ damage secondary to
systemic arterial hypertension. The eye is a target organ as well as an established prognostic indicator of
systemichypertension. Based on ophthalmoscopically visible alterations, several classifications, the majority of
them grading hypertensive fundus changes into four stages have been suggested. The recognition of
hypertensive retinopathy is important in cardiovascular risk stratification of hypertensive individuals. The
review evaluates the changing perspectives in classification & prognostic significance of fundal lesions.
Keywords: Hypertensive Retinopathy;Classification; Attenuation; Haemorrhage; Hard exudates.

I. Introduction
Hypertensive Retinopathy was first described in 1859 by Liebreich(1).Hypertensive Retinopathy
consists of retinal vascular changes that are pathologically related to both transient & persistent microvascular
damage from elevated blood pressure. Ocular changes can be the initial finding in an asymptomatic patient with
hypertension necessitating primary referral. In other instances, asymptomatic patient may be referred to an
ophthalmologist for visual problems caused by hypertensive changes. Elevation of systemic blood pressure
causes both focal and generalized constriction of retinal arterioles mediated by autoregulation. These findings
are relatively common in long standing hypertension. A prolonged duration of high blood pressure can be
associated with a breakdown of inner blood retinal barrier with extravasation of plasma & RBCs . Retinal
haemorrhages, cotton wool spots, intraretinal lipids & in severe cases , the development of macular star
configuration of intraretinal lipid can be seen. Although its name implies only retinal involvement, changes in
both choroid & optic nerve are observed. When choroidal vessels are severely affected by elevated blood
pressure, as in acute hypertension, fibrinoid necrosis of choroidal arterioles can cause occlusion of areas of
choriocapillaris, with a subsequent breakdown of outer blood retinal barrier. Ocular findings in accelerated
hypertension are divided into three distinct categories: hypertensive retinopathy, hypertensive choroidopathy &
hypertensive optic neuropathy.
Ophthalmic findings in acute malignant hypertensive retinopathy include focal arterial narrowing,
cotton wool spots, intraretinal transudates , macular edema and retinal haemorrhages. Cystoid macular edema,
lipid deposits and arteriolar changes are signs of malignant hypertensive retinopathy(2). Cotton wool spots are
fluffy, elevated, tan white areas of retinal opacity occurring within a few disc diameters of optic nerve, caused
by occlusion of terminal retinal arterioles. Cotton wool spots typically resolve in 3-6 weeks and are associated
with permanent nerve fiber layer loss in the vicinity of the lesion(2). Periarteriolar intraretinal transudates are tan
white retinal lesions which resolve without residual retinal damage in 2-3 weeks(3). Macular edema and
subretinal fluid are retinal findings related to hypertensive choroidal changes affecting the retinal pigment
epithelium, with alterations in the blood retinal barrier. Clinical changes from hypertensive choroidopathy are
directly related to the release of endogenous vasoconstrictor agents (eg.,angiotensin II, epinephrine, vasopressin)
during systemic hypertension. Angiographically, there is delayed, patchy choroida lfilling(2). Gitter et al
demonstrated through the use of fluorescein angiography that delay in choroidal filling is followed by late
leakage from choroidal vessels into the subretinal space(4). The leakage is enhanced by infarction and damage to
the RPE cells or transudation of fluid to subretinal space in response to increase pressure in the choroidal
vessels(5). Focal occlusion of the choriocapillaris leads to necrosis & atrophy of the RPE, forming Elschnigs
spots(6). Subretinal fluid accumulates , with the eventual formation of macular edema, a common finding
associated with hypertensive choroidopathy(3). Hypertensive optic neuropathy presents clinically as disc edema.
This occurs from vasoconstriction of the posterior ciliary arteries supplying the optic nerve head, resulting from
the release of angiotensin II and other vasoconstricting agents. In many cases, hypertensive changes are not
extensive enough to induce breakdown of either the inner or outer blood retinal barrier. Instead, the chronic
effects of hypertension on the retinal vessels become intimately associated with arteriosclerosis changes in the
retina characterised by vascular thickening. Hypertensive arteriosclerosis refers to the progressive increase in
the elastic & muscular components of wall of arteriole induced by hypertension. With long standing
hypertension , elastic tissue forms multiple concentric layers in intima of the arteriole. The muscular layer can
be replaced by collagen fibers & the intima can be replaced by hyaline thickening.
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Changing Perspectives in Classifications of Hypertensive Retinopathy.

With advancing age, however similar changes can develop in the absence of systemic hypertension, these are
termed as senile or involutional arteriosclerosis. These changes are accelerated by hypertension. Changes in the
retinal circulation in the acute phase of hypertension primarily involve the terminal arterioles. Acute
hypertension of any cause can enter into an accelerated or malignant stage, characterized by the fibrinoid
necrosis of the arterioles with papilloedema(7). Main retinal arteriolar changes are seen & recognize as a
response to chronic systemic hypertension.
Increased thickening of arteriolar wall caused by arteriosclerotic process causes progressive changes in
the appearance of the light reflex from arteriole. Normally the arteriolar wall is invisible, only the column of
RBCs in the lumen is visible as the red line we recognize as the vessel. Reflection of the incident light from the
convex surface of the normal arteriolar wall causes a thin line of reflected light to appear in the middle of blood
column, the normal light reflex. As the wall becomes thickened, the light reflex loses its brightness & becomes
somewhat broader & more diffuse in appearance. This is the earliest sign of arteriosclerosis.
With increasing thickness of arteriolar wall & decreasing lumen, there is further diffusion of the light
from the arteriole & the light reflex takes on the reddish brown hue of the copper wire reflex. As the process
continues, there is further thickening of arteriolar wall with associated reduction in the lumen, when the column
of blood can no longer be visualized even as a thin line, the arteriole assumes the appearance of silver wire.
Arteriosclerotic thickening of the vessel wall also affects the appearance of A-V crossing. The arteriole &
venule share a common adventitial sheath when they cross, with venule lying anterior. Both vascular sclerosis &
perivascular glial cell proliferation contribute to the compression of venule & constriction of its lumen ,causing
appearance of A-V nicking. Seitz attributed the crossing phenomenon to vascular sclerosis & perivascular glial
cell proliferation & not to venous compression(8). This venous compression varies in severity, from very mild
tapering of venous blood column, to more severe tapering, to interruption of visible blood column. The sclerotic
changes can also cause deflection of venule as it crosses the arteriole at an acute angle. With increasing sclerotic
changes, the venule assumes a more obtuse angle with respect to arteriole at the common crossing & in severe
cases it crosses the arteriole at right angle. Retinal macroaneurysms may also be associated with hypertension.
In a reviewof 120 patients with retinal arterial macroaneurysms 67% had hypertension(9).
The traditional classification of hypertensive retinopathy proposed by Keith et al in 1939 was an
attempt to show that severity of hypertension itself was predictive of mortality(10). This classification & its
modifications typically consist of four grades of hypertensive retinopathy with increasing severity. The major
limitation of this classification system is the difficulty in distinguishing early hypertensive retinopathy severity
(ie grade 1 from grade 2). Several proposals for a new systems have been made(11,12,13). Current literature
challenges the prognostic significance of early grade classifications of hypertensive retinopathy by KeithWagener-Barker and Scheie(14,15).
II. Discussion
In clinical routine, the widespread classification of Keith-Wagener-Barker 1939 has been a standard
for grading fundus changes in patients with arterial hypertension. The poor correlation with severity of
hypertension, variation in the onset & progression of clinical signs & recognition of optic neuropathy &
choroidopathy as independent entities have prompted some investigators to stress the importance of describing
fundal appearance rather than assigning a grade.
Keith Wagener classification is not very helpful as it combines changes of both arteriosclerosis &
hypertension.In 1953, Scheie separately classified arteriosclerotic & hypertensive changes(8). Both
classifications are given in Table 1.
Table 1 Classifications of hypertensive retinopathy: KeithWagener-Barker (grade IIV) was based on the level
of severity of the retinal findings; and Scheie (grade 04) attempted to quantify the changes of both
hypertension and arteriolosclerosis.
Grade
I
II
III
IV

KeithWagener-Barker
Features
Mild generalised retinal arteriolar narrowing
Definite focal narrowing and arteriovenous
nipping
The above and retinal haemorrhages, exudates
and cotton-wool spots
Grade III and papilloedema

Grade
0
1
2
3
4

Scheie
Features
No changes
Barely detectable arterial narrowing
Obvious arterial narrowing with focal
irregularities plus light reflex changes
Grade 2 plus copper wiring and retinal
haemorrhages/exudate
Grade 3 plus silver wiring and papilloedema

Scheie classification is also in adequate because Pickering pointed out that cotton wool spots are more ominous
prognostically than lipid exudation which is another stage 3 change. Also arteriolar changes vary depending
upon the previous presence of ageing changes in the vessel i.e involutional sclerosis. Leischman noted that prior
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Changing Perspectives in Classifications of Hypertensive Retinopathy.

sclerosis of arteriole seemingly prevented severe arteriolar constriction that occurs as a result of high blood
pressure & reported that it can protect the vessels from severe changes of malignant hypertension. (In young
patients with toxaemia of pregnancy or an abrupt elevation of blood pressure related to renal disease , sclerotic
changes are not present , pure hypertensive microangiopathy i.e narrowing is observed whereas in chronic
hypertension sclerotic changes appear).
Another classification system is the Neubauer Classification system which.is the modification of Keith
Wagener system which distinguishes mild (stage1 - 2) from severe form (stage3-4). Table2
Table 2 Neubauer classification of hypertensive fundus changes
Stage I
Optic Disc
Major retinal vessels
Arterioles
Precapillaries
Veins
Venules
Capillaries
Parenchyma
Stage II
Optic Disc
Major retinal vessels

Arterioles

Precapillaries
Veins
Venules
Capillaries
Parenchyma

Stage III
Optic Disc
Major retinal vessels
Arterioles
Precapillaries
Veins
Venules
Capillaries
Parenchyma

Stage IV

Normal, mild hyperaemia

Normal , barely detectable light reflex changes
Barely detectable arteriolar narrowing
Normal
Mild enlargement (eventually)
Mild tortuosity (eventually)
Visible on the optic disc
Normal

Normal, mild hyperaemia

Obvious increased light reflex changes, obvious narrowing of
vessel wall with focal irregularities
Obvious narrowing of vessel wall with focal or continuous
irregularities, obvious increased light reflex changes
Narrowed , irregular light reflexes
Mild enlargement (eventually)
Mild tortuosity
Few peripapillary loops
Mild haemorrhage, few cotton wool spots (eventually)

Often unsharply bordered , slightly prominent (eventually)

Mild to severe narrowing and focal constriction , irregular light
reflexes
Moderate to severe narrowing , irregular light reflexes
Narrowed , visible alterations of vessel walls
Mild enlargement (eventually)
Mild tortuosity
Ectatic
Focal & grouped haemorrhage , cotton wool spots ,
prethrombosis/thrombosis , capillary bleeding , hard(circinate)
exudates

Stage III + Papilloedema , peripapillary exudation; exudative retinal

detachment (eventually)

In 1996 Dodson proposed a classification consisting of only 2 grades: I (arteriolar narrowing, focal constriction
& A-V nicking) and II (haemorrhages & exudates with or without disc edema) (13). A similar classification has
been suggested to encourage the utilisation of the eye as a hypertensive target organ for risk stratification and
therapeutic decision making(17). Pache M in 2002 indicated significant angiographic difference between mild &
severe form of hypertensive retinopathy ie.significant rarefaction of perifoveal capillary bed & decrease in
capillary blood velocity, however unlike in ophthalmoscopy a differentiated division into four stages is not
possible(18).
The above explained heterogenous classifications of hypertensive retinopathy, making severity staging
a largely arbitrary process, as well as the lack of well defined prognostic value for either systemic outcomes or
visual impairment lead to recently proposed Wong classification ( Table 3) based on the concept that an
assessment of retinal vascular changes may provide further information for vascular risk stratification in persons
with hypertension. Wong formulated 3 grade classification system for hypertensive retinopathy & suggested
approach for patients with each grade
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Changing Perspectives in Classifications of Hypertensive Retinopathy.

Patients with mild HR signs require routine care & BP control should be based on established guidelines.
Patients with moderate HR signs (Retinal haemorrhage, cotton wool spots ,hard exudates) may benefit from
further assessment of vascular risk eg assessment of cholesterol levels & if clinically indicated, appropriate
risk reduction therapy(cholesterol lowering agents)

Patients with accelerated hypertension (bilateral disc swelling in presence of moderate hypertensive
retinopathy) will continue to need urgent immediate antihypertensive management, including possible
administration of IV medications.
Table 3 Classification of hypertensive retinopathy by Wong & Mitchell

Retinopathy Description

Systemic associations

Mild

One or more of the following signs: generalized arteriolar

narrowing, focal arteriolar narrowing, AV nicking, arteriolar wall
opacity (silver-wiring)

Weak associations with stroke, coronary heart disease

and cardiovascular mortality

Moderate

Mild retinopathy with one or more of the following signs: retinal

haemorrhages (blot, dot or flame-shaped), microaneurysms,
cotton-wool spot, hard exudates

Strong association with stroke, congestive heart failure,

renal dysfunction and cardiovascular mortality

Accelerated Moderate retinopathy signs plus optic disk swelling; may be

associated with visual loss

Associated with mortality and renal failure

III. Conclusion
The original classification system for hypertensive retinopathy was conceived in 1939 by Keith &
colleagues. Since then ,there have been several criticisms of the original system concerning the reproducibility
& the relevance of the system to clinical practice. Subsequently, there have been other classification systems
proposed & focus is towards how does the physician use these data.A clinical assessment of hypertensive
retinopathy signs may therefore provide more accurate cardiovascular risk stratification & potentially guiding
treatment strategies.

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